The present study demonstrated that diltiazem may be more repressive than nicardipine against the acute surge of NA and DP in patients with SAH. NA and DP are mainly derived from sympathetic nerve endings [5] and our findings support the notion that diltiazem exerted inhibitory effects on the sympathetic nervous system. The primary action of Ca²⁺ channel blockers is to inhibit the Ca²⁺ influx through voltage-dependent calcium channels in the plasma membrane that leads to relaxation and vasodilation of vascular smooth muscle [1]. Previous studies have shown that the inhibition of Ca²⁺ channels can decrease catecholamine release by inhibiting neurotransmitter release at adrenergic nerve terminals [6, 11]. Several authors reported that diltiazem might have an inhibitory effect on sympathetic transmission through some extra actions in addition to the inhibition of Ca²⁺ influx into the adrenergic nerve endings [8, 16], although the mechanism remains to be elucidated.

We have demonstrated previously that AD concentrations were markedly high immediately after SAH onset and decreased rapidly, whereas NA and DP concentrations had a significant time delay until their peak occurred compared with AD [17, 19]. The discrepancy of response to diltiazem among catecholamines may arise from the difference in the time course of when diltiazem affects the activated sympathetic nervous system. Further controlled clinical trials are needed to establish the beneficial effect of diltiazem in patients with aneurysmal SAH.